Using design thinking to create and implement a 3D digital library of anatomical specimens.

Design thinking (DT) is a five-stage process (empathize, define, ideate, prototype, and test) that guides the creation of user-centered solutions to complex problems. DT is in common use outside of science but has rarely been applied to anatomical education. The use of DT in this study identified the need for flexible access to anatomical specimens outside of the anatomy laboratory and guided the creation of a digital library of three-dimensional (3D) anatomical specimens (3D Anatomy Viewer).

A workflow for the creation of photorealistic 3D cadaveric models using photogrammetry.

Three-dimensional (3D) representations of anatomical specimens are increasingly used as learning resources. Photogrammetry is a well-established technique that can be used to generate 3D models and has only been recently applied to produce visualisations of cadaveric specimens. This study has developed a semi-standardised photogrammetry workflow to produce photorealistic models of human specimens.

Towards developing standard operating procedures for pre-clinical testing in the mdx mouse model of Duchenne muscular dystrophy.

This review discusses various issues to consider when developing standard operating procedures for pre-clinical studies in the mdx mouse model of Duchenne muscular dystrophy (DMD). The review describes and evaluates a wide range of techniques used to measure parameters of muscle pathology in mdx mice and identifies some basic techniques that might comprise standardised approaches for evaluation. While the central aim is to provide a basis for the development of standardised procedures to evaluate efficacy of a drug or a therapeutic strategy, a further aim is to gain insight into pathophysiological mechanisms in order to identify other therapeutic targets.

Three-dimensional optical coherence tomography of whole-muscle autografts as a precursor to morphological assessment of muscular dystrophy in mice.

Three-dimensional optical coherence tomography (3D-OCT) is used to evaluate the structure and pathology of regenerating mouse skeletal muscle autografts for the first time. The death of myofibers with associated inflammation and subsequent new muscle formation in this graft model represents key features of necrosis and inflammation in the human disease Duchenne muscular dystrophy. We perform 3D-OCT imaging of excised autografts and compare OCT images with coregistered histology.

Implications of cross-talk between tumour necrosis factor and insulin-like growth factor-1 signalling in skeletal muscle.

1. Inflammation, particularly the pro-inflammatory cytokine tumour necrosis factor (TNF), increases necrosis of skeletal muscle. Depletion of inflammatory cells, such as neutrophils, cromolyn blockade of mast cell degranulation or pharmacological blockade of TNF reduces necrosis of dystrophic myofibres in the mdx mouse model of the lethal childhood disease Duchenne muscular dystrophy (DMD).

Reduced muscle necrosis and long-term benefits in dystrophic mdx mice after cV1q (blockade of TNF) treatment.

Tumour necrosis factor (TNF) is a potent inflammatory cytokine that appears to exacerbate damage of dystrophic muscle in vivo. The monoclonal murine specific antibody cV1q that specifically neutralises murine TNF demonstrated significant anti-inflammatory effects in dystrophic mdx mice. cV1q administration protected dystrophic skeletal myofibres against necrosis in both young and adult mdx mice and in adult mdx mice subjected to 48 h voluntary wheel exercise.

Reduced necrosis of dystrophic muscle by depletion of host neutrophils, or blocking TNFalpha function with Etanercept in mdx mice.

Necrosis of skeletal muscle fibres in the lethal childhood myopathy Duchenne Muscular Dystrophy results from deficiency of the cell membrane associated protein, dystrophin. We test the hypothesis in dystrophin-deficient mice, that the initial sarcolemmal breakdown resulting from dystrophin deficiency is exacerbated by inflammatory cells, specifically neutrophils, and that cytokines, specifically Tumour Necrosis Factor alpha (TNFalpha), contribute to myofibre necrosis. Antibody depletion of host neutrophils resulted in a delayed and significantly reduced amount of skeletal muscle breakdown in young dystrophic mdx mice.

Cromolyn administration (to block mast cell degranulation) reduces necrosis of dystrophic muscle in mdx mice.

Duchenne muscular dystrophy is a lethal muscle wasting disorder, resulting from mutations in the gene encoding for the skeletal muscle protein dystrophin. The absence of functional dystrophin leaves the muscle membrane vulnerable to damage during contraction. Damage initially occurs as 'tears' in the membrane, this damage can be exacerbated by the inflammatory response leading to myofibre necrosis rather than repair.